MINISTRY OF PUBLIC HEALTH OF UKRAINE ZAPOROZHE STATE MEDICAL UNIVERSITY DEPARTMENT OF GENERAL PRACTICE – FAMILY MEDICINE

EMERGENCY IN THE PRACTICE OF FAMILY DOCTOR

THE TEXTBOOK FOR THE PRACTICAL CLASSES AND INDIVIDUAL WORK FOR 6TH-YEARS STUDENTS OF INTERNATIONAL FACULTY (SPECIALITY «GENERAL MEDICINE») DISCIPLINE: «GENERAL PRACTICE – FAMILY MEDICINE»

Content module 3

Zaporozhye, 2015

Approved by: MoH of Ukrainе protocol № 2, the 16.06.2015 y.

Readers: Chuhrienko N.D. – Doctor of Medical Sciences, Professor of Family Medicine department, Dnepropetrovsk State Medical Academy MoH of Ukraine; Kuryata O.V. – Doctor of Medical Sciences, Professor, head of Hospital therapy № 1 and profpathology department, Dnepropetrovsk State Medical Academy MoH of Ukraine.

Writers: Mykhailovska N.S. – Doctor of Medical Sciences, Professor, head of General practice – family medicine department, Zaporozhye State Medical University; Grytsay A.V. – PhD, associate professor of General practice – family medicine department, Zaporozhye State Medical University.

Methodical recommendations compiled in accordance with the program of «General practice - family medicine». Guidelines are intended to help students prepare for practical classes and learn the material. Can be used for training of 6th-years students of international faculty, discipline «General practice - family medicine».

Zaporozhye state medical university Publishing office of ZSMU

2 CONTENT

The thematic plan of practical classes…………………………………………….. 5 The thematic plan of independent work of student………………………………. 7 TOPIC 5. The emergency in the practice of family doctor. The emergency in the pre-hospital stage in the case of cardiac arrest, acute coronary syndrome, respiratory standstill, arrhythmias, hypertensic crisis, bronchoobstructive syndrome…………………………………………...... 8 TOPIC 6. The emergency in the practice of family doctor in the case of pain syndrome. The clinical classification of pain. The mechanism of pain in incurable patient. The principles of treatment of chronic pain syndrome. The emergency in context of incurable diseases and imminent death………………………………………………………………………. 35 TOPIC 7. The emergency in the practice of family doctor in the case of seizure, syncope, coma in case of diabetes, acute hepatic failure, alcohol intoxication, renal insufficiency, narcotic abuse……………………….. 80 TOPIC 8. The emergency in the practice of family doctor in the case of bite, sting, electrical injury, drowning, frostbite and thermal injury…………………. 132 Recommended literature………………………………………………………….. 163

3 PREFACE

The family doctor has to provide emergency in the case of different life-threatening conditions: cardiac arrest, respiratory standstill, bronchoobstructive syndrome, hypertensic crisis, and pain. The timely diagnostics and ability to provides emergency at the pre-admission stage by family doctor, during transportation of the patient prevents complications, improves the treatment outcomes. This textbook includes the general principles and algorithms of emergency in the practice of family doctor in the case of pain. The necessity of this textbook is conditioned by absence of such workbooks, which satisfy requirements of basic parts of academic discipline «General practice – family medicine». This textbook is recommended for 6th-years students of Institute of higher education III-IV level of accreditation, speciality 7.12010001 «General medicine», training line 1201 «Medicine» studying related topics, interns, general practitioners, other specialists.

4 THE THEMATIC PLAN OF PRACTICAL CLASSES Module 1: «The organizational aspects of the system of the primary health care in Ukraine, its role in the development and reforming of the Public health».

Number № Topic of hours

Content module 1. Modern approaches to the medico-social and organizational basis of a primary health care 1 The place of the family medicine in the structure of a healthcare system 7 and the principles of the family service. The organization of the FD’s work. The basis recording documentation of FD in medical institution. The role of information system in FD practice. The basis of information processing of out-patient clinic.

Content module 2. Medico-social aspects of population‘s health - the basis of the preventive and curing medicine 2 Medico-social aspects of the population’s health. The medical 6 examination of the population, and rehabilitation in the family doctor’s practice. Medical insurance structure and family doctor activity. The models of medical insurance in the world.

3 3.1. The assessment of the risk factors of the main chronic non-epidemic 4 diseases and the preventive measures in case of the cardiovascular, bronchopulmonary, gastrointestinal diseases and some other common syndromes. A role of family doctor in popularization of healthy life style and prophylaxis. The dietotherapy. “The health school”. 3.2. The prophylaxis of AIDS. 2

4 4.1. The organization of out-of-hospital therapeutic help in case of the 2 most wide-spread diseases. The principles of medico-social expertise. The organization of the day hospital and home care. 4.2. The consultation in the context of HIV-infectious, voluntary testing. 2 4.3. The consultation in the context of incurable disease and imminent death. The organization of medical care for non-curable patients. The 2 principle of multidisciplinary approach to medical care of non-curable patients and their relatives. Nursing, the methods of palliative care of symptoms and syndromes.

Content module 3. The emergency in the family doctor’s practice.

5 Number № Topic of hours 5 The emergency in the practice of family doctor. The emergency in the 6 pre-hospital stage in the case of cardiac arrest, acute coronary syndrome, respiratory standstill, arrhythmias, hypertensic crisis, bronchoobstructive syndrome. 6 6.1.The emergency in the practice of family doctor in the case of pain 4 syndrome. 6.2.The clinical classification of pain. The mechanism of pain in 2 incurable patient. The principles of treatment of chronic pain syndrome. The emergency in context of incurable diseases and imminent death.

7 The emergency in the practice of family doctor in the case of seizure, 6 syncope, coma in case of diabetes, acute hepatic failure, alcohol intoxication, renal insufficiency, narcotic abuse. 8 The emergency in the practice of family doctor in the case of bite, sting, 5 electrical injury, drowning, frostbite and thermal injury. Final module control. 2 TOTAL 50

6 THE THEMATIC PLAN OF INDEPENDENT WORK OF STUDENT Number № Тopic Control type of hours 1. Preparation to the practical classes, the academic 20 level and training of practical skills 2. The implementation and defense of the practical 4 tasks

3. Filling of the family doctor’s documentation 3 Current control 4. The preparation and writing of the program of 4 during practical treatment in out-patient in the case of most classes widespread diseases 5. Drew up the algorithms of the pre-admission 4 emergency in the family doctor’s practice 6. The report at a clinical conference of hospitals. 1 7. Preparation for the final module control 4 Final module control Total 40

7 TOPIC 5 The emergency in the practice of family doctor. The emergency in the pre- hospital stage in the case of cardiac arrest, acute coronary syndrome, respiratory standstill, arrhythmias, hypertensic crisis, bronchoobstructive syndrome. І. Theme actuality According to official data, sudden death cases are about 10% among all reasons of death. In developed countries every year dies suddenly a lot of people: in the U.S. – 330 000, in Russia -300 000 persons. According to U.S. statistics, 250 000 cases of sudden death occurring at home, at work, in urban centers and only 80 000 cases - in hospitals. It was found that leading cause of sudden death is ventricular fibrillation. ІІ. Study purposes: to know clinical presentations of sudden death and the first aid on the pre-admission stage. ІІІ. Concrete purposes of the module:  To know the organization and content of out-patient clinic;  To identify diseases that require emergency care;  To be able to assess the state of patient and provide appropriate medical care in the case of major syndromes which requiring urgent medical assistance of family doctor;  To be able to perform cardiopulmonary resuscitation: the restoration of patency of airways, to correct arrhythmias, defibrillation. IV. A student must be able:  To know the basic diseases that may complicate the development of sudden death;  To know the principles of restoration of passable respiratory tract;  To know the technique of closed-chest cardiac massage;  To explain the mechanism of respiration;  To know the algorithm of defibrillation. V. Task for initial independent training 1. At the first defibrillation attempt in adult the electric discharge is: A. 400 J B. 250 J C. 200 J D. 360 J E. 300 J

8 2. The most effective method of urgent ventilation is: A. Rhythmical chest compression B. mouth-to-mouth method C. Sylvester’s method D. Holger-Nielsen’s method E. Ambu’s bag

3. After a primary cardiac arrest consciousness disappears through: А. 10-15 sec B. 2 min. C. 15-20 sec D. 1 min. E. 30 sec

4. The most common cause of sudden death is: A. Hypertensive crisis B. central nervous system lesion C. Acute hemorrhage D. Disease of cardiovascular system E. Cancer

5. What is the primary symptom for diagnose the circulatory arrest? A. Convulsion B. Absence of heart sounds by auscultation C. Absence of carotid pulsation D. midriatic pupils E. Absence of spontaneous breathing

6. During cardiopulmonary resuscitation the electrical defibrillation is shown by: A. izoline B. irregular waves C. nodal rhythm D. Always circulatory arrest E. sinus bradycardia

9 7. Asystole is the same as: A. Absence of systolic blood pressure B. Collapse C. complete atrioventricular heart block D. Cardiac arrest E. Syncope

8. What is the most frequent complication of resuscitation measures in elderly patients? A. hepatorrhexis B. Spine Fractures C. Gaps lung D. jawfall E. Fractures of ribs and sternum

9. More often sudden death occurs as a result: A. The asystole B. development of atrioventricular dissociation C. ventricular fibrillation D. atrial fibrillation E. Ventricular tachycardia

10. Identify the share of cases without morphologic signs in heart in the case of sudden death A. 5-7% B. 10-15% C. 20-26% D. 12% E. 20%

Answers: 1 2 3 4 5 6 7 8 9 10 C B A D C B D E C D

10 VI. Basic questions after a theme Basic principles of emergency providing in the rural and urban area, the role of FD. The importance of timely medical care to reduce mortality and disability. The share of sudden death in the mortality structure. The causes of sudden death. The types of circulatory arrest. Supplemental investigation for determine types of circulatory arrest. Methodology of emergency care in the case of circulatory arrest, respiratory standstill, traumatic death. Independent work: preparation to practical studies - 4 hours. VII. The plan and organizational structure of practical training. Educational materials Place of Hours, № Stage Facilities realization of min Equipment of studies studies Control of initial 15 min Tests Classroom 1 level 2 Analysis of theme 90 min Oral test Classroom Practical work 115 min Out-patients Family out-patient's 3 case record clinic Current control 15 min Situational Classroom 4 of knowledge tasks Summation 5 min Classroom 5 of studies Independent work 4 hours The individual Classroom preparation to 6 practical studies

VIII. The content of theme Сardiovascular collapse, cardiac arrest, and sudden cardiac death The vast majority of naturally occurring sudden deaths are caused by cardiac disorders. The magnitude of the problem of cardiac causes is highlighted by estimates that more than 300,000 sudden cardiac deaths (SCD) occur each year in the U.S., as many as 50% of all cardiac deaths. SCD is a direct consequence of cardiac arrest, which is often reversible if responded to promptly. Since resuscitation techniques and emergency rescue systems are available to save patients who have out-of-hospital

11 cardiac arrest, which was uniformly fatal in the past, understanding the SCD problem has practical importance. SCD must be defined carefully. In the context of time, «sudden» is defined, for most clinical and epidemiologic purposes, as 1 h or less between the onset of the terminal clinical event and death. An exception is unwitnessed deaths in which pathologists may expand the definition of time to 24 h after the victim was last seen to be alive and stable [9]. Because of community-based interventions, victims may remain biologically alive for days or weeks after a cardiac arrest that has resulted in irreversible central nervous system damage. Confusion in terms can be avoided by adhering strictly to definitions of death, cardiac arrest, and cardiovascular collapse, as outlined in Table 1. Death is biologically, legally, and literally an absolute and irreversible event. Death may be delayed in a survivor of cardiac arrest, but "survival after sudden death" is contradictory. Currently, the accepted definition of SCD is natural death due to cardiac causes, heralded by abrupt loss of consciousness within 1 h of the onset of acute symptoms, in an individual who may have known preexisting heart - disease but in whom the time and mode of death are unexpected. When biologic death of the cardiac arrest victim is delayed because; interventions, the relevant pathophysiologic event remains the sudden and unexpected cardiac arrest that leads ultimately to death, even though delayed by artificial methods. The language used should reflect the fact that the index event was a cardiac arrest and that death was due to its delayed consequences [15]. Etiology, initiating events, and clinical epidemiology Extensive epidemiologic studies have identified populations at high risk for SCD. In addition, a large body of pathologic data provides information on the underlying structural abnormalities in victims of SCD, and clinical/physiologic studies have begun to identify a group of transient functional factors that may convert a long-standing under-lying structural abnormality from a stable to an unstable state (Table 2). This information is developing into an understanding of the causes and mechanisms of SCD. Cardiac disorders constitute the most common causes of sudden natural death. After an initial peak incidence of sudden death between birth and 6 months of age (the sudden infant death syndrome), the incidence of sudden death declines sharply and remains low through childhood and adolescence. The incidence begins to increase in young adults, reaching a second peak in the age range of 45 to 75 years. Increasing age in this range is a powerful risk factor for sudden cardiac death, and the proportion of 12 cardiac causes among all sudden natural deaths increases dramatically with advancing years. From 1 to 13 years of age, only one of five sudden natural deaths is due to cardiac causes. Between 14 and 21 years of age, the proportion increases to 30%, and then to 88% in the middle-aged and elderly [7,10]. Young and middle-aged men and women have very different susceptibilities to SCD, but the gender differences decrease with advancing age. Table 1 Distinction Between Death, Cardiac Arrest, and Cardiovascular Collapse

Term Definition Qualifiers or Exeptoins Death Irreversible cessation of all None biologic functions Cardiac arrest Abrupt cessation of cardiac pump Rare spontaneous reversions; function which may be reversible likelihood of successful by a prompt intervention but will interventions; relates to lead to death in its absence mechanism of arrest and clinical setting Cardiovascular A sudden loss of effective blood Nonspecific term which collapse flow due to cardiac and/or includes cardiac arrest and its peripheral vascular factors which consequences and also events may reverse spontaneously (e.g., which characteristically revert neuro-cardiogenic syncope; spontaneously vasovagal syncope) or only with interventions (e.g., cardiac arrest)

The overall male/female ratio is approximately 4:1, but in 45 to 64-year-old age group, the male SCD excess is nearly 7:1. It falls to approximately 2:1 in the 65- to 74-year-old age group. The difference in risk for SCD parallels the risks for other manifestations of coronary heart disease (CHD) in men and women. As the gap for other manifestations of coronary heart disease closes in the seventh and eighth decades of life, the excess risk of SCD also narrows. Despite the lower incidence in women, the classic coronary risk factors still operate in women – cigarette smoking, diabetes, hyperlipidemia, hypertension – and SDC remains an important clinical and epidemiologic problem [7,8]. Hereditary factors contribute to the risk of SCD, but largely in a nonspecific manner: they represent expressions of the hereditary predisposition to CHD. Except for a few specific syndromes, such as the genetic hyperlipoproteinemias, congenital long

13 QT interval syndromes, and a number of myopathic and dysplastic syndromes there are no specific hereditary risk factors for SCD. The major categories of structural causes of, and functional factors contributing to, the SCD syndrome are listed in Table 2. Worldwide, and especially in western cultures, coronary atherosclerotic heart disease is the most common structural abnormality associated with SCD. Up to 80% of all SCDs in the U.S. are due to the consequences of coronary atherosclerosis. The cardiomyopathies (dilated and hypertrophic, collectively) account for another 10 to 15% of SCDs, and all the remaining diverse etiologies cause only 5 to 10% of these events. Transient ischemia in the previously scarred or hypertrophied heart, hemodynamic and fluid and electrolyte disturbances, fluctuations in autonomic nervous system activity, and transient electrophysiologic changes caused by drugs or other chemicals (e.g., proarrhythmia) have all been implicated as mechanisms responsible for transition from electrophysiologic stability to instability. In addition, spontaneous reperfusion of ischemic myocardium, caused by vasomotor changes in the coronary vasculature and/ or spontaneous thrombolysis, may cause transient electrophysiologic instability and arrhythmias [16]. Pathology. Data from postmortem examinations of SCD victims parallel the clinical observations on the prevalence of CHD as the major structural etiologic factor. More than 80% of SCD victims have pathologic findings of CHD. The pathologic description often includes a combination of long-standing, extensive atherosclerosis of the epicardial coronary arteries and acute active coronary lesions, which include a combination of fissured or ruptured plaques, platelet aggregates, hemorrhage, and thombosis. In one study, chronic coronary atherosclerosis involving two or more major vessels with >75% stenosis was observed in 75% of the victims. In another study, atherosclerotic plaque assuring, platelet aggregates, and/or acute thrombosis were observed in 95 of 100 individuals who had pathologic studies after SCD. Most of these acute changes were superimposed on preexisting chronic lesions. As many as 70 to 75% of males who die suddenly have prior myocardial infarctions (Mis), but only 20 to 30% have recent acute Mis. A high incidence of left ventricular (LV) hypertrophy coexists with prior Mis [7,12]. Clinical definition of forms of cardiovascular collapse (Table 1). Cardiovascular collapse is a general term connoting loss of effective blood flow due to acute dysfunction of the heart and/or peripheral vasculature. Cardiovascular collapse may be caused by vasodepressor syncope (vasovagal syncope, postural 14 hypotension with syncope, neurocardiogenic syncope), a transient severe bradycardia, or cardiac arrest. The latter is distinguished from the transient forms of cardiovascular collapse in that it usually requires an intervention to achieve resuscitation. In contrast, vasodepressor syncope and many primary bradyarrhythmic syncopal events are transient and non-life-threatening, and the patient will regain consciousness spontaneously [15,16]. The most common electrical mechanism for true cardiac arrest is ventricular fibrillation (VF), which is responsible for 65 to 80% of cardiac arrests. Severe persistent bradyarrhythmias, asystole, and pulseless electrical activity (an organized electrical activity without mechanical response - formerly called electomechanical dissociation) cause another 20 to 30%. Sustained ventricular tachycardia (VT) with hypotension is a less common cause. Acute low cardiac output states, having precipitous onset, also may present clinically as a cardiac arrest. The causes include massive acute pulmonary emboli, internal blood loss from ruptured aortic aneurysm, intense anaphylaxis, cardiac rupture after myocardial infarction, and unexpected fatal arrhythmia due to electrolyte disturbances. Table 2 Cardiac Arrest and Sudden Cardiac Death Structural causes I. Coronary heart disease A. Coronary artery abnormalities 1. Chronic atherosclerotic lesions 2. Acute (active) lesions (plaque assuring, platelet aggregation, acute thrombosis) 3. Anomalous coronary artery anatomy B. Myocardial infarction 1. Healed 2. Acute II. Myocardial hypertrophy A. Secondary B. Hypertrophic cardiomyopathy 1. Obstructive 2. Nonobstructive III. Dilated cardiomyopathy - primary muscle disease IV. Inflammatory and infiltrative disorders 15 A. Myocarditis B. Noninfectious inflammatory diseases C. Infiltrative diseases V. Valvular heart disease VI. Electrophysiologic abnormalities, structural A. Anomalous pathways in Wolff-Parkinson-White syndrome B. Conducting system disease C. Membrane channel structure (e.g., congenital long QT syndrome) Functional contributing factors I. Alterations of coronary blood flow A. Transient ischemia B. Reperfusion after ischemia II. Low cardiac output states A. Heart failure 1. Chronic 2. Acute decompensation B. Shock III. Systemic metabolic abnormalities A. Electrolyte imbalance (e.g., hypokalemia) IV. Neurophysiologic disturbances A. Autonomic fluctuations: central, neural, humoral B. Receptor function V. Toxic responses A. Proarrhythmic drug effects B. Cardiac toxins (e.g., cocaine, digitalis intoxication) C. Drug interactions

Clinical characteristics of cardiac arrest Prodrome, onset, arrest, death. SCD may be presaged by days, weeks, or months of increasing angina, dyspnea, palpitations, easy fatigability, and other nonspecific complaints. However, these prodromal complaints are generally predictive of any major cardiac event; they are not specific for predicting SCD [7,17]. The onset of the terminal event, leading to cardiac arrest, is defined as an acute change in cardiovascular status preceding cardiac arrest by up to 1 h. When the onset is instantaneous or abrupt, the probability that the arrest is cardiac in origin is >95%. 16 Continuous ECG recordings, fortuitously obtained at the onset of a cardiac arrest, commonly demonstrate changes in cardiac electrical activity in the minutes or hours before the event. There is a tendency for the heart rate to increase and for advanced grades of premature ventricular contractions (PVCs) to evolve. Most cardiac arrests that occur by the mechanism of VF begin with a run of sustained or nonsustained VT, which then degenerates into VF. Sudden unexpected loss of effective circulation may be separated into «arrhythmic events» and «circulatory failure». Arrhythmic events are characterized by a high likelihood of patients being awake and active immediately prior to the event, are dominated by VF as the electrical mechanism, and have a short duration of terminal illness (<1 h). In contrast, circulatory failure deaths occur in patients who are inactive or comatose, have a higher incidence of asystole than VF, have a tendency to a longer duration of terminal illness, and are dominated by noncardiac events preceding the terminal illness [9]. The onset of cardiac arrest may be characterized by typical symptoms of an acute cardiac event, such as prolonged angina or the pain of onset of MI, acute dyspnea or orthopnea, or the sudden onset of palpitations, sustained tachycardia, or light- headedness. However, in many patients, the onset is precipitous, without forewarning. Cardiac arrest is, by definition, abrupt. Mentation may be impaired in patients with sustained VT during the onset of the terminal event. However, complete loss of consciousness is a sine qua non in cardiac arrest. Although rare spontaneous reversions occur, it is usual that cardiac arrest progresses to death within minutes (i.e., SCD has occurred) if active interventions are not undertaken promptly. The ability to resuscitate the victim of cardiac arrest is related to the time from onset to institution of resuscitative efforts, the setting in which the event occurs, the mechanism (VF, VT, pulseless electrical activity, asystole), and the clinical status of the patient prior to the cardiac arrest. Those settings in which it is possible to institute prompt cardiopulmonary resuscitation (CPR) provide a better chance of a successful outcome. The outcome in intensive care units and other in-hospital environments is heavily influenced by the patient's preceding clinical status. The immediate outcome is good for cardiac arrest occurring in the intensive care unit in the presence of an acute cardiac event or transient metabolic disturbance, but the outcome for patients with far- advanced chronic cardiac disease or advanced noncardiac diseases (e.g., renal failure, pneumonia, sepsis, diabetes, cancer) is no more successful in hospital than in the out-of- hospital setting [10]. 17 The success rate for initial resuscitation and ultimate survival from an out-of- hospital cardiac arrest depends in part on the mechanism of the event. When the mechanism is VT, the outcome is best (67%); VF is the next most successful (25%), and asystole and pulseless electrical activity generate dismal outcome statistics. Advanced age also influences adversely the chances of successful resuscitation. Progression to biologic death is a function of the mechanism of cardiac arrest and the length of the delay before interventions. VF or asystole, without CPR within the first 4 to 6 min, has a poor outcome, and there are few survivors among patients who had no life-support activities for the first 8 min after onset. Outcome statistics are improved considerably by lay bystander intervention (basic life support) prior to definitive interventions (advanced life support - defibrillation) and by early defibrillation. Death during the hospitalization after a successfully resuscitated cardiac arrest relates closely to the severity of central nervous system injury. Anoxic encephalopathy and infections subsequent to prolonged respirator dependence account for 60% of the deaths. Another 30% occur as a consequence of low cardiac output states that fail to respond to interventions. Paradoxically, recurrent arrhythmias are the least common cause of death, accounting for only 10% of in-hospital deaths [8-11]. Among patients who have cardiac arrest in the setting of acute MI, it is important to distinguish between primary and secondary cardiac arrests. Primary cardiac arrests refer to those that occur in the absence of hemodynamic instability, and secondary cardiac arrest are those that occur in patients in whom abnormal hemodynamics dominate the clinical picture before cardiac arrest. The success rate for immediate resuscitation in primary cardiac arrest during acute MP in a monitored setting should approach 100%. In contrast, as many as 70% of patients with secondary cardiac arrest succumb immediately or during the same hospitalization. Identification of patients at risk for sudden cardiac death. Primary prevention of cardiac arrest depends on the ability to identify individual patients at high risk. One must view the problem in the context of the total number of events and the population pools from which they are derived. The annual incidence of SCD among an unselected adult population is 1 to 2 per 1000 population, largely reflecting the prevalence of those CHD patients among whom SCD is the first clinically recognized manifestation (20 to 25% of first coronary events are SCD). The incidence (percent per year) increases progressively with addition of identified coronary risk factors to populations free of prior coronary events. The most powerful factors are age, elevated blood pressure, LV hypertrophy, cigarette smoking, elevated serum cholesterol level, obesity, and 18 nonspecific electrocardiographic abnormalities. These coronary risk factors are not specific for SCD but rather represent increasing risk for all coronary deaths. The proportion of coronary deaths that are sudden remains at approximately 50% in all risk categories. Despite the marked relative increased risk of SCD with addition of multiple risk factors (from 1 to 2 per 1000 population per year in an unselected population to as much as 50 to 60 per 1000 in subgroups having multiple risk factors for coronary artery disease), the absolute incidence remains relatively low when viewed as the relationship between the number of individuals who have a preventive intervention and the number of events that can be prevented. Specifically, a 50% reduction in annual SCD risk would be a huge relative decrease but would require an intervention in up to 200 unselected individuals to prevent one sudden death. These figures highlight the importance of primary prevention of CHD. Control of coronary risk factors may be the only practical method to prevent SCD in major segments of the population, because of the paradox that the majority of events occur in the large unselected subgroups rather than in the specific high-risk subgroups. Under most conditions of higher level of risk, particularly those indexed to a recent major cardiovascular event (e.g., MI, recent onset of heart failure, survival after out-of-hospital cardiac arrest), the highest risk of sudden death occurs within the initial 6 to 18 months and then decreases toward baseline risk of the underlying disease. Accordingly, preventive interventions are most likely to be effective when initiated early [7-9]. For patients with acute or prior clinical manifestations of CHD, high-risk subgroups having a much higher ratio of SCD risk to population base can be identified. The acute, convalescent, and chronic phases of MI provide large population subsets with more highly focused risk. The potential risk of cardiac arrest from the onset through the first 72 h after acute MI (the acute phase) may be as high as 15 to 20%. The highest risk of SCD in relation to MI is found in the subgroup that has experienced sustained VT or VF during the convalescent phase (3 days to 8 weeks) after MI. A greater than 50% mortality in 6 to 12 months has been observed among these patients, when managed with conservative medical therapy, and at least 50% of the deaths are sudden. Since the development of aggressive intervention techniques, the incidence appears to have fallen dramatically. After the acute phase of MI, long-term risk for total mortality and SCD are predicted by a number of factors. The most important for both SCD and non-SCD is the extent of myocardial damage sustained during the acute event. This is measured by the degree of reduction in the ejection fraction (EF), functional capacity, and/or the 19 occurrence of heart failure. Increasing frequency of postinfarction PVCs, with a plateau above the range of 10 to 30 PVCs per hour on 24-h ambulatory monitor recordings, also indicates increased risk, but advanced forms (salvos, nonsustained VT) are probably the more powerful predictor. PVCs interact strongly with decreased left ventricular EF. The combination of frequent PVCs, salvos or nonsustained VT, and an EF<30% identifies patients who have an annual risk of 20%. The risk falls off sharply with decreasing PVC frequency and the absence of advanced forms, as well as with higher EF. Despite the risk implications of postinfarction PVCs, improved outcome as a result of PVC suppression has not been demonstrated. The extent of underlying disease due to any cause and/or prior clinical expression of risk of SCD (i.e., survival after out-of-hospital cardiac arrest not associated with acute MI) identify patients at very high risk for subsequent (recurrent) cardiac arrest. Survival after out-of-hospital cardiac arrest predicts up to a 30% 1-year recurrent cardiac arrest rate in the absence of specific interventions [10]. A general rule is that the risk of SCD is approximately one-half the total cardiovascular mortality rate. Thus, the SCD risk is approximately 20% per year for patients with advanced CHD or dilated cardiomyopathy severe enough to result in a 40% 1-year total mortality rate. The very high risk subgroups provide more focused population fractions («Percent/Year») for predicting cardiac arrest or SCD; but the impact on the overall population («Events/Yea») is considerably smaller. The requirements for achieving a major population impact are effective prevention of the underlying diseases and/or new epidemiologic probes that will allow better resolution of subgroups within large general populations. Treatment. The individual who collapses suddenly is managed in four stages: 1) the initial response and basic life support, 2) advanced life support, 3) postresuscitation care, 4) long-term management. The initial response and basic life support can be carried out by physicians, nurses, paramedical personnel, and trained lay persons. There is a requirement for increasing skills as the patient moves through the stages of advanced life support, postresuscitation care, and long-term management [7,16]. Initial Response and Basic Life Support. The initial response will confirm whether a sudden collapse is indeed due to a cardiac arrest. Observations for respiratory movements, skin color, and the presence or absence of pulses in the carotid or femoral 20 arteries will promptly determine whether a life-threatening cardiac arrest has occurred. As soon as a cardiac arrest is suspected or confirmed, contacting an emergency rescue system (e.g., 911) should be the immediate priority. Agonal respiratory movements may persist for a short time after the onset of cardiac arrest, but it is important to observe for severe stridor with a persistent pulse as a clue to aspiration of a foreign body or food. If this is suspected, a prompt Heimlich maneuver may dislodge the obstructing body. A precordial blow, or "thump," delivered firmly by the clenched fist to the junction of the middle and lower third of the sternum may occasionally revert VT or VF, but there is concern about converting VT to VF. Therefore, it has been recommended to use precordial thumps as an advanced life support technique when monitoring and defibrillation are available. This conservative application of the technique remains controversial [9]. The third action during the initial response is to clear the airway. The head is tilted back and chin lifted so that the oropharynx can be explored to clear the airway. Dentures or foreign bodies are removed, and the Heimlich maneuver is performed if there is reason to suspect that a foreign body is lodged in the oropharynx. If respiratory arrest precipitating cardiac arrest is suspected, a second precordial thump is delivered after the airway is cleared. Basic life support, more popularly known as CPR, is intended to maintain organ perfusion until definitive interventions can be instituted. The elements of CPR are the establishment and maintenance of ventilation of the lungs and compression of the chest. Mouth-to-mouth respiration may be used if no specific rescue equipment is immediately available (e.g., plastic oropharyngeal airways, esophageal obturators, masked Ambu bag). Conventional ventilation techniques during CPR require the lungs to be inflated 10 to 12 times per minute, i.e., once every fifth chest compression when two persons are performing the resuscitation and twice in succession every 15 chest compressions when one person is carrying out both ventilation and chest wall compression[8]. Chest compression is based on the assumption that cardiac compression allows the heart to maintain a pump function by sequential filling and emptying of its chambers, with competent valves maintaining forward direction of flow. The palm of one hand is placed over the lower sternum, with the heel of the other resting on the dorsum of the lower hand. The sternum is depressed, with the arms remaining straight, at a rate of approximately 80 to 100 per minute. Sufficient force is applied to depress the sternum 3 to 5 cm, and relaxation is abrupt.

21 Advanced Life Support is intended to achieve adequate ventilation, control cardiac arrhythmias, stabilize the hemodynamic status (blood pressure and cardiac output), and restore organ perfusion. The activities carried out to achieve these goals include: 1) intubation with an endotracheal tube, 2) defibrillation/cardioversion and/or pacing, 3) insertion of an intravenous line.

Ventilation with O2 (room air if O2 is not immediately available) may promptly reverse hypoxemia and acidosis. The speed with which defibrillation/cardioversion is carried out is an important element for successful resuscitation. When possible, immediate defibrillation should precede intubation and insertion of an intravenous line; CPR should be carried out while the defibrillator is being charged. As soon as a diagnosis of VT or VF is obtained, a 200-J shock should be delivered. Additional shocks at higher energies, up to a maximum of 360 J, are tried if the initial shock does not successfully abolish VT or VF. Epinephrine 1 mg intravenously is given after failed defibrillation, and attempts to defibrillate are repeated. The dose of epinephrine may be repeated after intervals of 3 to 5 min [8,9]. If the patient is less than fully conscious upon reversion, or if two or three attempts fail, prompt intubation, ventilation, and arterial blood gas analysis should be carried out. Intravenous NaHCO3, which was formerly used in large quantities, is no longer considered routinely necessary and may be dangerous in larger quantities. However, the patient who is persistently acidotic after successful defibrillation and intubation should be given 1 meq/kg NaHCO3 initially and an additional 50% of the dose repeated every 10 to 15 min. After initial unsuccessful defibrillation attempts, or with persistent electrical instability, a bolus of 1 mg/kg lidocaine is given intravenously, and the dose is repeated in 2 min in those patients who have persistent ventricular arrhythmias or remain in VF. This is followed by a continuous infusion at a rate of 1 to 4 mg/min. If lidocaine fails to provide control, intravenous procainamid (loading infusion of 100 mg/5 min to a total dose of 500 mg, followed by continuous infusion at 2 to 5 mg/min) or bretylium tosylate (loading dose 5 to 10 mg/kg in 5 min; maintenance dose 0,5 to 2 mg/min) may be tried. Intravenous calcium gluconate is no longer considered safe or necessary for routine administration. It is used only in patients in whom acute hyperkalemia is known to be the triggering event for resistant VF, in the presence of know, hypocalcemia, or in patients who have received toxic doses of calcium channel antagonists [12]. 22 Cardiac arrest secondary to bradyarrhythmias or asystole is mail aged differently. Once it is known that this type of rhythm is presell there is no role for external shock. The patient is promptly intubate CPR is continued, and an attempt is made to control hypoxemia and acidosis. Epinephrine and/or atropine are given intravenously or an intracardiac route. External pacing devices are now available to attempt to establish a regular rhythm, but the prognosis is generally very poor in this form of cardiac arrest. The one exception is bradyrhythmic/asystolic cardiac arrest secondary to airway obstruction This form of cardiac arrest may respond promptly to removal foreign bodies by the Heimlich maneuver or, in hospitalized patients, by intubation and suctioning of obstructing secretions in the airway [14]. Postresuscitation Care is defined by the clinical setting of the cardiac arrest. Primary VF acute MI is generally very responsive to life-support, techniques and easily controlled after the initial event. Patients are maintained on a lidocaine infusion at the rate of 2 to 4 mg/min for 24 to 72 h after the event. In the in-hospital setting, respirator support is usually not necessary or is needed for only a short time, and hemodynamics stabilize promptly after defibrillation or cardioversion In secondary VF in acute MI (those events in which hemodynamic abnormalities predispose to the potentially fatal arrhythmia), resuscitative efforts are less often successful, and in those patients who are successfully resuscitated, the recurrence rate is high. The clinical picture is dominated by hemodynamic instability. In fact, the outcome is determined more by the ability to control hemodynamic dysfunction than by electrophysiological abnormalities. Bradyarrhythmias, asystole, and pulseless electrical activity are commonly secondary events in hemodynamically unstable patients and are less responsive to interventions. The outcome after in-hospital cardiac arrest associated with non-cardiac diseases is poor, and in the few successfully resuscitated patients, the postresuscitation course is dominated by the nature of the underlying disease. Patients with cancer, renal failure, acute central nervous system disease, and uncontrolled infections, as a group, have a survival rate of less than 10% after in-hospital cardiac arrest. Some major exceptions are patients with transient airway obstruction, electrolyte disturbances, proarrhythmic effects of drugs, and severe metabolic abnormalities, most of whom may have an excellent chance of survival if they can be resuscitated promptly and maintained while the transient abnormalities are being corrected [13]. Long-Term Management after Survival of Out-of-Hospital Cardiac Arrest Patients who do not suffer irreversible injury of the central nervous system and who achieve hemodynamic stability should have extensive diagnostic and therapeutic testing 23 to guide long-term management. This aggressive approach is driven by the fact that statistics from the 1970s indicated survival after out-of- hospital cardiac arrest was followed by a 30% recurrent cardiac arrest rate at 1 year, 45% at 2 years, and a total mortality rate of almost 60% at 2 years. Historical comparisons suggest that these dismal statistics may be significantly improved by newer interventions, but the magnitude of the improvement is unknown because of the lack of concurrently controlled intervention studies [12]. Among those patients in whom an acute transmural MI is the cause of out-of- hospital cardiac arrest, the management is the same as in any other patient who suffers cardiac arrest during the acute phase of a documented MI. For almost all other categories of patients, however, extensive diagnostic studies are carried out to determine etiology, functional impairment, and electrophysiologic instability as guides to future management. In general, patients who have out-of-hospital cardiac arrest due to chronic ischemic heart disease, without an acute MI, are evaluated to determine whether transient ischemia or chronic electrophysiological instability was the more likely cause of the event. If there is reason to suspect an ischemic mechanism, coronary revascularization or drugs, most commonly beta blockers, are used to reduce ischemia. Electrophysiological instability is best identified by the use of programmed electrical stimulation to determine whether sustained VT or VF can be induced. If so, this information can be used as a baseline against which to evaluate drug efficacy for prevention of inducibility or to determine suitability for map-guided antiarrhythmic surgery, or whether an implantable cardiovertor/defibrillator (ICD) might be the best strategy. Using this technique in patients with EF of 30% or more, the recurrent cardiac arrest rate is less than 10% during the first year of follow-up when inducibility is suppressed by a drug. The outcome is not as good for patients with EF under 30% but may be still better than the apparent natural history of survival after cardiac arrest. For patients for whom successful drug therapy cannot be identified by this technique, insertion of an ICD, antiarrhythmic surgery (e.g., coronary bypass surgery, aneurysmectomy, cryoablation), or empiric amiodarone therapy can be considered options. Primary surgical success, defined as surviving the procedure and reverting to a noninducible status without drug therapy, is better than 90% when patients are selected for ability to be mapped in the operating room. However, only a small fraction of patients meet the criteria. In addition, VT/VF cannot be induced in a number of survivors of cardiac arrest (30 to 50%), and inducible arrhythmias can be suppressed by drugs in no more than 20 to 30% of those whose arrhythmias can be induced. Because 24 of these limitations of drug therapy and surgical approaches, ICD therapy has evolved into the most commonly used strategy for cardiac arrest survivors. ICDs have very good success rates for sensing and reverting life-threatening arrhythmias, but improvement in long-term total survival outcomes remains ill defined [15]. The ESVEM study has suggested that ambulatory monitor-based suppression of ambient arrhythmias is equivalent to electrophysiologically guided testing in predicting long-term outcome.

25 Algorithm of cardiopulmonary resuscitation (CPR) on the pre-admission stage

I. Found a person without movement, without respond to any irritants

Check airway, assess the adequacy of breathing

Check the heart rate during 10 seconds

Pulse is absent Pulse is felt

Start of CPR: 30 compressions of chest - Every 5-6 seconds - an inspiration, 2 inspiration check pulse every 2 minutes.

Actions are continued till appearance of Actions are continued till appearance cardiac activity and independent breathing of self-breathing

Actions are stopped after 30 minutes in the absence of cardiac activity and independent breathing.

II. The person suddenly loses consciousness

Check for carotid pulsation (during 5-7 seconds)

No pulsation

put hand on the bottom of the sternum

Check carotid pulsation

Presence of pulsation No pulsation

Observation of pulsation and breathing Start of CPR: 30 compressions of chest - 2 inspiration.

26 Cardiovascular Emergencies – Any condition that lead to respiratory impairment: reducing ability to deliver oxygen – Severe bleeding: Shock – Stroke: Reducing cerebral blood flow – Heart diseases: Reducing of tissue oxygenation – Heart attack: Can lead to cardiac arrest – Ventricular fibrillation: Heart muscle flutters rather than pumping blood Causes of circulatory arrest Cardiac • Ischemic heart disease (myocardial infarction, stenocardia) • Arrhythmias • Electrolytic disorders • Valvular disease • Cardiac tamponade • Pulmonary embolism • aortic aneurysm rupture Extracardiac • airway obstruction • acute respiratory failure • shock • reflectory cardiac arrest • embolisms of different origin • drug overdose • electric injury • poisoning Sequence of actions:  Check responsiveness  Call for help  Correct position of patient and ensure the open airway  Check the presence of spontaneous respiration  Check peripheral pulsation  Start closed-chest massage and artificial ventilation

27 Main stages of resuscitation: A (Airway) – ensure open airway by preventing the falling back of tongue, tracheal intubation if possible; B (Breathing) – start artificial lungs ventilation; C (Circulation) – restore the circulation by closed-chest massage; D (Differentiation, Drugs, Defibrillation) – quickly perform differential diagnosis of circulatory arrest, use different medication and electric defibrillation in case of ventricular fibrillation.

28 Algorithm of cardiopulmonary resuscitation

29 IX. Tasks for final control 1. During cardiopulmonary resuscitation should be observed the following rules: A. Head should be dropped B. Head should be elevated C. Compressed abdominal aorta D. Whatever surface on which the patient lies E. The patient should be ventilate by pure oxygen

2. Which of the following symptoms is the indication for closed-chest massage? A. The absence of peripheral arteries pulsation B. Midriatic pupils C. The absence of carotid pulsation D. Miotic pupils E. Cyanotic skin

3. The cause of circulatory arrest in diastole can be: A. Acidosis B. Hypokalemia C. Hypercalcemia D. Respiratory alkalosis E. Hypoglycemia

4. After a primary circulatory arrest spontaneous breathing stops after: A. 30 sec B. 20 sec C. 5 min. D. 60 sec E. 2 min.

5. In patients with absence of pulse asystole on ECG was diagnosed. Primary remedial measure should be: A. Electric defibrillation B. Adrenalin injection C. Atropine injection

30 D. Calcium chloride injection E. Lidocain injection

6. Which of the following medicines cannot be injected endotracheally during cardiopulmonary resuscitation? A. Lidocain B. Adrenalin C. Noradrenaline D. Atropine sulfate E. Calcium chloride

7. Define the correct ratio between the number of contractions of chest and the respiration number during cardiopulmonary resuscitation: A. 5:1 B. 12:2 C. 30:2 D. 24:2 E. 9:1

8. For effective closed-chest massage in adult patients, breast bone drifts toward the spine to: A. 1 - 2 cm B. 5 - 6 cm C. 7 - 8 cm D. 3 - 4 cm E. 8 - 9 cm

9. After injection of digoxin 0,75 mg the patient of 55 years old suddenly lost consciousness. Peripheric pulse was absent, agonal breathing, BP didn’t determined. What examination do you have to conduct during resuscitation? A. Heart radiokimography B. ECG C. Vektorcardiography D. Radiography of the chest E. Heart ultrasonography 31 10. Adrenaline injection to resume the cardiac function in the case of: A. Hyperglycemia B. Alkalosis C. Acidosis D. Hypokalemia E. Acid-base balance plasma does not matter Answers: 1 2 3 4 5 6 7 8 9 10 E C A D B E C D B C

X. Practical skills 1. 82 years old patient had circulatory arrest and respiratory standstill. Medical history: prolonged heart failure. On the 5th minute of cardiopulmonary resuscitation, which was started on time, there wasn’t the cardiac activity. What is the prognosis for further resuscitation? A. Full restoration is impossible B. Restoration of beatings with some extrasystoles C. Full recovery D. Full recovery with following deterioration E. Possible restore of sinus rhythm

2. There was an attack of rhythm disturbance in the patient: atrial fibrillation, paroxysm of ventricular tachycardia. Which universal antiarrhythmic is most reasonable for patient? A. Pananhin B. Procainamide hydrochloride C. Lidokain D. Verapamil E. Digoxin

3. On the fourth postoperational day the 68 years old patient had acute bradicardia with asystole, no consciousness, coarse breathing. Resuscitation was started. What is the criterion of effectiveness of resuscitation? A. xerophthalmus B. Appearance of breath C. Reduction of cyanosis

32 D. The carotid pulsation E. Myotic pupils

4. In-hospital 50 year old patient with arterial hypertension, ischemic heart disease suddenly fainted. Duty doctor diagnosed the circulatory arrest and respiratory standstill. The cardiopulmonary resuscitation was started. A set of false teeth was extracted. What will be the following actions? A. Intracardiac injection of adrenalin B. Intracardiac injection of atropine C. Closed-chest massage D. Proceed to ventilation E. Throw back patient's head, lift chin, pull and fix tongue

5. Man was injured as a result of falling from a height. Physical examination: no response to natural irritants, unconscious, no breathing, thready pulse, left foot was unnatural turn to the other side, numerous wounds and scratches on skin. Which are primary measures in this case? A. Applying of sterile bandages on wounds B. Immobilization of fractures C. Transfusion-infusion therapy D. Respiratory restoration E. Anesthesia

6. The 75-years-old man was unconscious in the street with no pulsation on main arteries, mydriatic pupils. The clinical death was diagnosed. Which are primary measures in this case? A. emergency call B. Start a closed-chest cardiac massage C. Start the cardiopulmonary resuscitation D. Elevate the lower limbs E. Start artificial respiration

7. Resuscitation of elderly patient was not effective: wave of artificial carotid pulsation was not determined; the closed-chest cardiac massage was performed with displacement of the lower half of the sternum on 2-3 cm toward the spine because of chest stiffness. When the heart massage will be effective? A. Increasing the displacement of sternum to 4-5 cm

33 B. Start the open-chest cardiac massage C. Perform chest compression in left parasternal region D. 10 ml 10% calcium chloride solution injection E. Increasing displacement of sternum to 6-7 cm

8. The patient suddenly turned pale, unconscious. The skin was cyanotic, no photoreaction, no carotid pulsation, asystole on ECG. Which are primary measures in this case? A. Precardiac blow В. Artificial respiration C. The closed-chest cardiac massage D. Droperidol injection E. Adrenaline injection

9. You perform the resuscitation measures for patient - closed-chest cardiac massage, mouth-to-mouth ventilation. Which will be duration of these actions in the absence of recovery of cardiac and central nervous system activity? A. 45 minutes B. Before the emergency arrival C. 60 minutes D. 30 minutes E. 15 minutes

10. During diagnostic endoscopy the 45-years-old patient was asystole on ECG. Which will be your primary action? A. Electrical cardiac acceleration B. Sodium bicarbonate injection C. Atropine injection D. defibrillation. E. closed-chest cardiac massage, artificial ventilation Answers: 1 2 3 4 5 6 7 8 9 10 C B C E C C A B D E

34 TOPIC 6 The emergency in the practice of family doctor in the case of pain syndrome. The clinical classification of pain. The mechanism of pain in incurable patient. The principles of treatment of chronic pain syndrome. The emergency in context of incurable diseases and imminent death. I. Theme actuality The task of medicine is to preserve and restore health and to relieve suffering. Understanding pain is essential to both these goals. Because pain is universally understood as a signal of disease, it is the most common symptom that brings a patient to a physician's attention. The function of the pain sensory system is to detect, localize, and identify tissue-damaging processes. Since different diseases produce characteristic patterns of tissue damage, the quality, time course, and location of a patient's pain complaint and the location of tenderness provide important diagnostic clues and are used to evaluate the response to treatment. II. Study purposes: to learn the basic organizational, diagnostic and therapeutic features of surgical patients (obstetrics and gynecology, surgery, traumatology and orthopedics, urology, proctology, oncology, ophthalmology, otolaryngology, dentistry, resuscitation and intensive therapy) in practice of FD; to diagnose the medical condition of pain in the chest, during initial contact with patient and determine the indications for urgent hospitalization in the pre-admission stage in the case of pain. III. Concrete purposes of the module: - to know the features inter-sectorial interrelation of FD in outpatient clinic; - to evaluate the benefits of the FD in the proceedings of preventive measures; - to identify diseases and conditions that require emergency care; - to assess the patient's condition and provide appropriate medical care in emergency case in FD practice; - to know dosage, indications and contraindications for drug in emergency case; - to identify emergency cases in FD practice.

IV. A student must be able: • to know the clinical presentations of disease with abdominal pain: acute appendicitis, pancreatitis, cholecystitis, peptic ulcer and its complications, acute gynecological diseases, ectopic pregnancy, renal colic, and inflammatory diseases of the kidneys and urinary tract.

35 • to know the clinical presentations of disease with chest pain: various forms of CHD, pericarditis, myocarditis, pulmonary embolism, dissecting aortic aneurysm, pneumothorax, dry pleurisy, lesions of peripheral nerves, spine and muscles. • to identify the acute coronary syndrome with ST segment elevation, ST-segment elevation without clinical characteristics of acute coronary syndrome, therapeutic approach of pre-admission and emergency care. • to know the characteristics of pain in the extremities and clinical signs of acute lesions of veins and arteries.

V. Task for initial independent training 1. The patient complaints for pain in the left upper quadrant of abdomen, weakness, vomiting, dizziness, which appeared 5 hours ago. Hypotension, tachycardia. Medical history: 10 days ago blunt trauma of abdomen. What is the working diagnosis? A. Rupture of the spleen; B. Rupture of the liver; C. Rupture of intestine; D. Peritonitis; E. Perforated ulcer. 2. 2 days ago the patient felt a sharp pain in the right upper quadrant of abdomen with irradiation under the right scapula. Next day he had vomiting. The right half of the abdomen is tense. Positive symptoms of Ortner, Musset. What is the working diagnosis? A. Acute pancreatitis; B. Mesenteric ischemia; C. Acute intestinal obstruction; D. Biliary colic; E. Acute cholecystitis.

3. In the case of angina the typical pain is: A. Pressing, squeezing, localized behind the breastbone. B. Burning heart pain. C. Barbed heart pain associated with movements or breathing. D. Feeling of discomfort in the pericardial region during physical or emotional stress. E. Feeling heterogonous object under the sternum.

36 4. The 21 years old patient admitted to the doctor. She complained for lower abdomen pain spreading to the anus, weakness, which came on the 12th day of the . BP 70/40 mm Hg, HR 120. What is the working diagnosis? A. ectopic pregnancy; B. Torsion of ; C. Acute appendicitis; D. Acute pelvioperitonit; E. Ovarian apoplexy.

5. The 43 years old patient complains for right lumbar pain spreading to the lower abdomen. Patient was motionless, groaning. HR 100, BP 130/70 mm Hg. The muscles tension in the right iliac region. Negative Lassega, Schetkina, Ortner signs. Positive Pasternatsky sign. What is the working diagnosis? A. perforated duodenal ulcer; B. Renal colic; C. Radiculitis; D. Acute appendicitis; E. Acute cholecystitis.

6. Dangerous electric current for human health is: A. Above 50 volts. B. Above 150 volts. C. Above 100 volts. D. Above 75 volts. E. Above 200 volts.

7. The sign of severe overheating of the body is: A. Body temperature of 40,5 C. B. Heart rate 130 per min. C. Reduced muscle tone. D. Body temperature 39,5 C. E. Heart rate 120 per min.

8. The skin lesions in the case of thermal most often determined by: A. «Rule of Donald». 37 B. «Rule of Nine». C. «Frank Rule». D. «Rule palm». E. Rule of thermal shock.

9. The sign of deep frostbite is: A. Pale skin. B. Cyanotic skin. C. Pale skin, soft tissue lying below. D. Heart rate 110/hv. E. None of the above.

10. The victim of hypothermia was admitted to the hospital. Rectal temperature was 32,0 C. What was degree of hypothermia? A. Severe. B. Light. C. Moderate. D. Deep. E. Coma. Answers: 1 2 3 4 5 6 7 8 9 10 A E A E B C A B E C

VI. Basic questions after theme • Surgical diseases, symptoms and syndromes, the prevention, diagnosis and treatment of patients by a family doctor. • Surgical diseases, symptoms and syndromes, which are the indication for refer to specialists for making final diagnosis, differential diagnosis, planning a therapeutic approach. • Surgical diseases, symptoms and syndromes, for which the FD may prescribe treatment and rehabilitation for patients according to the recommendations of specialists, may conduct clinical supervision under patients.

38 • Surgical diseases, symptoms and syndromes, which require FD and medical specialist’s supervision for implementation of working and final diagnosis, treatment, rehabilitation of patients. • Surgical diseases that require treatment and clinical supervision of doctors. • Surgical diseases that need emergency or planned hospitalization of patients. • Differential diagnosis of acute and chronic pain, somatic and psychosomatic disorders. • Diagnosis of pain in various clinical situations and treatment. • Method of patient’s help in the case of acute coronary syndrome at the pre- admission stage. • The therapeutic approach for patient with acute arterial occlusion. • Pathophysiological changes in the case of insects stinging, serpents, emergency. VII. Practical skills: The examination of patients in the surgical clinic by ophthalmologist, otolaryngologist, urologist, gynecologist or family doctor. In the case of pain propose the algorithms and differential diagnosis of medical care in the pre- admission stage. Independent work: compiling algorithms of emergency during practical classes - 6 hours.

VIII. The content of theme The pain sensory system. Pain is an unpleasant sensation localized to a part of the body. Chest discomfort and palpitation Chest discomfort is one of the most frequent complaints for which patients seek medical attention; the potential benefit (or harm) resulting from the proper (or improper) assessment and management of the patient with this complaint is enormous. Failure to recognize a serious disorder, such as ischemic heart disease, may result in the dangerous delay of much-needed treatment, while an incorrect diagnosis of a potentially hazardous condition such as angina pectoris is likely to have harmful psychological and economic consequences and may lead to unnecessary cardiac catheterization. There is little relation between the severity of chest discomfort and the gravity of its cause. Therefore, a frequent problem in patients who complain of chest discomfort or pain is distinguishing trivial complaints from coronary artery disease and other serious disorders (Table 1) [7].

39 Causes of chest discomfort. Discomfort due to Myocardial Ischemia. Discomfort due to myocardial ischemia occurs when the oxygen supply to the heart is deficient in relation to the oxygen need. The blood flow through the coronary arteries is directly proportional to the pressure gradient between the aorta and the ventricular myocardium (during systole) or the ventricular cavity (during diastole). However, in the presence of critical stenosis, it is also proportional to the fourth power of the radius of the coronary arteries. A relatively slight alteration in coronary luminal diameter below a critical level can produce a large decrease in coronary flow, provided that other factors remain constant. Coronary blood flow occurs primarily during diastole, when it is unopposed by systolic myocardial compression of the coronary vessels. Table 1 Some Causes of Chest Discomfort and the Types of Discomfort associated with Them New, acute, often Recurrent, Persistent, even Cause ongoing episodic for days CARDIAC Coronary artery disease + + - Aortic stenosis - + - Hypertropic - + - cardiomyopathy Pericarditis + + + VASCULAR Aortic dissection + - - Pulmonary embolism + + - Pulmonary hypertension + + - Right ventricular strain + + - PULMONARY Pleuritis or pneumonia + + + Tracheobronchitis + + + Pneumothorax + - + Tumor - - + Mediastinitis or + - + mediastinal emphysema GASTROINTESTINAL Esophogeal reflux + + + Esophogeal spasm + + + Mallory-Weiss tear + - - Peptic ulcer disease + + - Biliary disease + + - Pancreatitis + +

40 New, acute, often Recurrent, Persistent, even Cause ongoing episodic for days MUSCULOSKELETAL Cervical disk disease - + + Arthritis of the shoulder - + + or spine Costochondritis + + + Intercostal muscl